The long-term goals of this project are to characterize the mechanisms by which the central nucleus of amygdala (CEA) interacts with incentive motivational systems to mediate the acquisition and expression of cocaine self-administration (S-A). It is proposed that the effects of CEA manipulations are mediated by an interaction between the CEA and mesolimbic dopamine (DA) neurons known to project to the nucleus accumbens (ACB). To test this hypothesis, four sets of experiments are proposed: 1) To characterize the effects of CEA stimulation or inactivation on DA release and cocaine S-A; 2) To anatomically identify sites of CEA/ACB interactions that mediate these neurochemical and behavioral changes; 3) To investigate directly the contribution of mesolimbic DA neurons, with emphasis on A8 and its interaction with CEA, to DA release and cocaine S-A; and 4) To identify receptor mechanisms by which CEA interacts with midbrain DAergic neurons. Determining the circuits and mechanisms by which CEA interacts with DA neurons to modify behavior and modulate DA release within ACB is fundamental to understanding the neural representation of incentive motivation, but has paid special relevance for understanding how drugs of abuse gain control over behavior and can induce craving and relapse to drug use following prolonged abstinence.